Resistance against vaginal colonisation by in strain TO mice after exposure to the mycoplasma was investigated. Eighteen mice from which had been eliminated from the vagina, either naturally or by antibiotic therapy, were resistant to vaginal recolonisation. Specific antibody was measured by an indirect micro-immunofluorescence technique and the geometric mean titre (GMT) for each group of mice is presented. Almost all of 31 mice that had developed circulating antibody (GMT 83) or local antibody (GMT 40), or both, after vaginal exposure were resistant to re-colonisation, as were those in which antibodies could not be detected. Seven other mice which had been colonised only in the oropharynx previously and which possessed antibody—circulating (GMT 64) or local (GMT30), or both—were resistant to vaginal colonisation, but 13 mice with little or no antibody after lack of colonisation at either anatomical site were susceptible. All of 15 mice given killed organisms intravenously, despite developing circulating antibody in high titre (GMT 122), were susceptible to vaginal colonisation, as were 14 of 15 mice that developed circulating (GMT 15) and local antibodies after being given killed organisms intravaginally. However, 25 mice with high titres of circulating (GMT 154–170) or local (GMT 20) antibody, or both, after receiving live organisms intravenously, were less susceptible to vaginal colonisation (17 becoming colonised) than were 21 non-immunised mice (all becoming colonised) and the organisms were eradicated more rapidly from the former. Despite this, the mice that were colonised following intravenous inoculation of live organisms had pre-challenge antibody titres that were as great as those that were not colonised. The results indicate that vaginal protection is likely to be mediated by factors other than, or in addition to, antibody, presumably by a cell-mediated means, and that concurrent respiratory infections are likely to contribute to vaginal immunity.


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